Diabetic angiopathy including micro- and macroangiopathy is concerned with high rate of morbidity and mortality in patients with long-standing diabetes. Receptor for advanced glycation end products (RAGE) and its ligands have been considered as important pathogenic triggers for the progression of the vascular injuries in diabetes. The deleterious link between RAGE and diabetic angiopathy has been demonstrated in animal studies. Preventive and therapeutic strategies focusing on RAGE and its ligand axis may be of great importance in relieving diabetic vascular complications and reducing the burden of disease.

This study was conducted to investigate the mechanism of lead (Pb)-induced testicular toxicity. We examined the impact of Pb toxicity on 17β-oestradiol (E2), oestrogen receptors (ERs) and aromatase P450 which are key factors in spermatogenesis. Treatment of rats with Pb acetate (PbAc, 50 mg/L in drinking water) significantly reduced sperm count, motility, viability and increased sperm abnormalities along with degenerative changes in seminiferous tubules and Leydig cells. Additionally, administration of PbAc resulted in a significant reduction in serum testosterone, serum and testicular E2 as well as increased level of testicular testosterone. Pb also induced testicular oxidative stress as evidenced by a significant decrease in the activities of superoxide dismutase, glutathione peroxidase and catalase antioxidant enzymes, and increased malondialdehyde level in the testis. At the molecular level, Pb treatment downregulated the mRNA expression of P450 arom (Cyp19) and ERα. In conclusion, Pb induces testicular oxidative damage and disrupts spermatogenesis, at least in part, via downregulation of Cyp19 and ERα expression, which further decrease E2 level. These data, therefore, provide insight into the mechanism of lead-induced testicular toxicity.

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Abstract. Calligonum comosum (C. comosum) is an Egyptian desert plant that contains polyphenol antioxidants. The present study examined the chemopreventive effect of an extract of C. comosum in a rat model of hepatocarcinogenesis. Male Wistar rats (n=40) were administered 100 mg/kg diethylnitrosamine (DEN) by intraperitoneal (i.p.) injection once a week for 3 weeks. Subsequently, depending on whether the rats received further administration of 0.8 mg/kg carbon tetrachloride (CCl 4 ) i.p. once a week for 7 weeks and 100 mg/kg C. comosum extract in their diet for 7 weeks, the rats were divided into four groups as follows: Group 1, treatment with DEN alone; group 2, treatment with DEN and C. comosum extract; group 3, treatment with DEN and CCl 4 ; and group 4, treatment with DEN, CCl 4 and C. comosum extract. The supplementation of C. comosum extract significantly suppressed the elevation in serum liver enzyme levels, including aspartate aminotransferase, alanine transaminase and γ-glutamyl transferase, and reduced the degree of oval cell proliferation induced by DEN and CCl 4 . In addition, C. comosum extract significantly decreased the number and area of glutathione S-transferase placental form-positive preneoplastic hepatic foci induced by DEN, with or without CCl 4 treatment. To the best of our knowledge, the present study is the first to provide definitive evidence of the hepatoprotective and chemopreventive effects of C. comosum.